Arteri Koroner

Miokard
Atherosklerosis bahan lemak
terkumpul di lapisan sebelah
dalam dinding arteri
Aterosklerosis di arteri menuju
jantung (arteri koroner)penyakit
jantung koroner

Rasa tidak nyaman di dada yang

disebabkan oleh ischemia miokard tetapi
tidak sampai terjadi nekrosis.
Biasanya berkisar 1 15 menit di daerah
retrosternal, tetapi dapat juga menjalar ke
rahang, leher, bahu, punggung dan
lengan kiri.
Reseptor saraf nyeri terangsang oleh
metabolit yang tertimbun, stres mekanik
lokal
Penyebab nyeri: peningkatan kebutuhan
miokard akan oksigen. Hilang dengan
istirahat atau nitrogliserin

ETIOLOGI
Atherosklerosis
Aorta insufisiensi
Spasmus arteri koroner
Anemia berat
TIPE SERANGAN
Angina stabil, angina non stabil
Stable angina/effort angina
Unstable angina/crescendo angina

Angina stabil
Memiliki pola, dapat diprediksi, timbul saat kebutuhan oksigen jantung
meningkat
Contoh: aktivitas berat, terpapar dingin, emosi
Hilang dengan istirahat dan nitrogliserin
Angina tidak stabil
Tidak memiliki pola, bisa terjadi lebih sering dan lebih berat, dapat
terjadi dengan atau tanpa aktivitas. Istirahat dan nitrogliserin tidak
menghilangkan nyeri, diperlukan penatalaksanaan kegawatdaruratan
segera.
Variant (Prinzmetal's) Angina
Disebabkan spasme arteri koroner. Biasanya timbul sewaktu istirahat,
dan nyeri dapat menjadi lebih berat. Nitrogliserin dapat menghilangkan
nyeri

Nyeri dada substernal atau retrosternal menjalar ke leher, daerah inter

skapula atau lengan kiri.
Kualitas nyeri seperti tertekan benda berat, seperti diperas, terasa
panas, kadang-kadang hanya perasaan tidak enak di dada (chest
discomfort).
Nyeri hilang (berkurang) bila istirahat atau pemberian nitrogliserin.
Gejala penyerta: sesak nafas, perasaan lelah, kadang muncul keringat
dingin, palpitasi, dizziness.
Gambaran EKG : depresi segmen ST, terlihat gelombang T terbalik.
Gambaran EKG seringkali normal pada waktu tidak timbul serangan.

Saat serangan angina, bisa ditemukan adanya gallop,

murmur regurgitasi mitral, split S2 atau ronkhi basah basal
yang kemudian menghilang

EKG
Normal pada 50 % dari penderita dengan angina pectoris. Bisa
ditemukan depresi atau elevasi segmen ST
Foto thoraks
biasanya normal, lebih sering menunjukkan kelainan pada
riwayat infark miokard atau nyeri dada yang bukan berasal
dari jantung.
Uji latih beban
Angiografi koroner diagnostik

Tujuan utama penatalaksanaan angina pectoris :

o Mencegah terjadinya infark miokard dan nekrosis
o Mengurangi simptom dan frekuensi serta beratnya iskemi
Prinsip penatalaksanaan: meningkatkan pemberian oksigen
(dengan meningkatkan aliran darah koroner) dan
menurunkan kebutuhan oksigen (dengan mengurangi kerja
jantung).

Penyekat Beta
menurunkan kebutuhan oksigen miokard dengan cara menurunkan
frekuensi denyut jantung, kontraktilitas, tekanan di arteri dan peregangan
pada dinding ventrikel kiri.
atenolol, metoprolol, propranolol, nadolol.
Nitrat dan Nitrit
vasodilator endothelium
Nitrat menurunkan kebutuhan oksigen miokard melalui pengurangan
preload
Amil nitrit, ISDN, isosorbid mononitrat, nitrogliserin.

Kalsium Antagonis
menghambat masuknya kalsium melalui saluran kalsium, yang
akan menyebabkan relaksasi otot polos pembuluh darah
sehingga terjadi vasodilatasi pada pembuluh darah epikardial
dan sistemik.
Kalsium antagonis juga menurunkan kabutuhan oksigen
miokard dengan cara menurunkan resistensi vaskuler sistemik.
Golongan: amlodipin, bepridil, diltiazem, felodipin, isradipin,
nikardipin, nifedipin, nimodipin, verapamil.

Terapi Farmakologis untuk mencegah Infark miokard akut

Terapi antiplatelet: aspirin, diberikan pada penderita PJK baik
akut atau kronik, kecuali ada kontra indikasi, penderita dapat
diberikan ticlopidin atau clopidogrel.
Terapi antikoagulan: heparin dan warfarin. Dosis rendah akan
menurunkan resiko terjadinya iskemia pada penderita dengan
faktor resiko .
Terapi penurunan kolesterol, simvastatin akan menurunkan
LDL ( low density lipoprotein ) sehingga memperbaiki fungsi
endotel pada daerah atheroskelerosis

Revaskularisasi Miokard
Angina pektoris dapat menetap sampai bertahun-tahun
dalam bentuk serangan ringan yang stabil.
Namun bila menjadi tidak stabil, episode nyeri menjadi lebih
sering dan berat, tanpa penyebab yang jelas.
Bila gejala tidak dapat dikontrol dengan terapi farmakologis
yang memadai, maka tindakan invasif seperti PTCA
(angioplasty coroner transluminal percutan) dipertimbangkan
untuk memperbaiki sirkulasi koronaria.

Pathway
Faktor resiko (merokok, hiperlipidemi,
ras, usia, dll)
Atherosklerosis
koroner
Penyumbatan arteri koroner
Stenosis aorta,
insufisiensi,
spasme, hipotensi,
anemia berat

Iskemi
miokardium

Metabolisme
anaerob
Asam laktat

Kontraktilitas
menurun

Nyeri
akut

Penurunan curah
jantung
Penurunan perfusi jaringan
Intoleransi aktivitas

Perfusi jaringan tidak efektif

rusaknya jaringan jantung akibat suplai darah yang tidak adekuat

suatu keadaan nekrosis miokard akibat aliran darah ke otot jantung
terganggu.
Iskemi lebih dari 30-45 menit terjadi kerusakan seluler ireversibel dan
kematian otot (nekrosis) bagian yang nekrosis akan berhenti
berkontraksi
Biasanya menyerang ventrikel kiri
Jenis sesuai letak, ex : anterior ventrikel kiri, inferior, septum, dll
Letak infark berkaitan gangguan sirkulasi koroner
Contoh : Lesi arteri koroner kanan infark dinding inferior

1. Suplai oksigen ke miokard berkurang yang disebabkan:

Adanya penyempitan arteri koroner akibat penebalan pada
dinding pembuluh darah, atherosklerosis, vasospasme,
emboli dan trombus
Faktor sirkulasi: hipotensi, stenosis aorta, insufisiensi
2. Kebutuhan oksigen miokard meningkat pada:
Hipertropi miokard
Hipertensi diastolik

Tidak bisa diubah: usia > 40thn, jenis kelamin, ras,

hereditas
Bisa diubah: hiperlipidemi, hipertensi, merokok,
diabetes, obesitas, diet tinggi lemak jenuh

Derajat gangguan fungsional tergantung :

Ukuran infark
Lokasi infark
Fungsi miokardium yang tak terlibat
Sirkulasi kolateral
Mekanisme kompensasi kardiovaskuler
Akibat dari infark:
Daya kontraksi menurun
Perubahan daya kembang dinding ventrikel
Pengurangan curah sekuncup

Infark Miokard yang disebabkan trombus arteri koroner dapat mengenai

endokardium sampai epikardium,disebut infark transmural.
Bisa juga hanya mengenai daerah subendokardial,disebut infark
subendokardial.
Setelah 20 menit terjadinya sumbatan,infark sudah dapat terjadi pada
subendokardium,dan bila berlanjut terus rata-rata dalam 4 jam telah
terjadi infark transmural.
Kerusakan miokard dari endokardium ke epikardium menjadi komplit dan
ireversibel dalam 3-4 jam.
Meskipun nekrosis miokard sudah komplit,proses remodeling miokard
yang mengalami injury terus berlanjut sampai beberapa minggu atau
bulan karena daerah infark meluas dan daerah non infark mengalami
dilatasi

Manifestasi Klinis

Gejala Klinis yang khas: nyeri dada retrosternal, seperti diremasremas dan tertekan, nyeri dapat menjalar ke lengan (kiri), bahu,
leher, rahang bahkan ke punggung dan epigastrium.
Nyeri berlangsung lebih lama dari angina pektoris dan tidak
responsif terhadap nitrogliserin.
Biasanya disertai perasaan mual, muntah, sesak, pusing,
keringat dingin, berdebar-debar, atau penderita sering ketakutan.
Takikardi, kulit dingin dan hipotensi ditemukan pada kasus yang
relatif lebih berat.
Dispneu

Meningkatnya kadar enzim jantung yang dilepaskan oleh

sel miokardium yang nekrosis : CK/CPK, SGOT/GOT,LDH
Pelepasan isoenzim MB-CK petunjuk yang lebih spesifik
Perubahan EKG : Q patologis, T inverted, elevasi segmen
ST
Gelombang Q nekrosis miokardial
Segmen ST dan Gelombang T iskemi menghilang
sesudah jangka waktu tertentu

Pada pemeriksaan EKG:

Fase hiperakut (beberapa jam permulaan serangan)
Elevasi yang curam dari segmen ST
Gelombang T yang tinggi dan lebar
Gelombang Q tampak
Fase perkembangan penuh (1-2 hari kemudian)
Gelombang Q patologis
Elevasi segmen ST yang cembung ke atas
Gelombang T yang terbalik
Fase resolusi
Gelombang Q patologis tetap ada
Segmen ST mungkin sudah kembali isoelektris
Gelombang T mungkin sudah menjadi normal

Lokasi infark miokard

berdasarkan perubahan
gambaran EKG:
No

Lokasi

Gambaran EKG

Anterior

Elevasi segmen ST dan/atau gelombang Q di

V1-V4/V5

Anteroseptal

Elevasi segmen ST dan/atau gelombang Q di

V1-V3

Anterolateral

Elevasi segmen ST dan/atau gelombang Q di

V1-V6 dan I dan aVL

Pada pemeriksaan darah (enzim jantung: CK, LDH)

Creatinin kinase (CK) meningkat pada 6-8 jam setelah awitan
infark dan memuncak antara 24 dan 28 jam pertama. Pada 2-4
hari setelah awitan menjadi normal
CK-MB meningkat setelah 3-6 jam
Nilai normal: <10 U/L
Dehidrogenase laktat (DH) mulai tampak pada serum setelah 24
jam pertama setelah awitan dan akan tinggi selama 7-10 hari
Nilai normal : 80-240 U/L

1.
2.
3.
4.
5.
6.
7.
8.

Gagal jantung kongestif

Syok kardiogenik
Defek septum ventrikel
Ruptur jantung
Aneurisme ventrikel
Tromboembolisme
Perikarditis
Aritmia

Penatalaksanaan
Pembatasan perluasan Infark Miokard
Pemberian obat-obat trombolitik (streptokinase)
Pemberian obat penghambat adrenoreseptor-beta untuk
pencegahan sekunder pasca infark.
Resusitasi jantung
Istirahat total
Oksigenasi
Obat untuk menghilangkan nyeri

Pathway
Faktor resiko (merokok, hiperlipidemi,
ras, usia, dll)
Aterosklerosis
korner
Penyumbatan arteri
koroner
Stenosis aorta,
insufisiensi,
spasme, hipotensi,
anemia berat

iskemi
Infark
miokard
Kontraktilitas
menurun

Metabolisme
anaerob
Asam laktat
Nyeri
akut

Penurunan curah
jantung
Penurunan perfusi
jaringan
Intoleransi aktivitas

Perfusi jaringan perifer tidka

NSTEMI vs STEMI
NSTEMI: NonST-segment elevation myocardial infarction
STEMI: ST-segment elevation myocardial infarction
NSTEMI account for about 30% and STEMI about 70% of

all heart attack (myocardial infarction)

NSTEMI occurs by developing a complete occlusion of a
minor coronary artery or a partial occlusion of a major
coronary artery previously affected by atherosclerosis. This
causes a partial thickness damage of heart muscle.
STEMI occurs by developing a complete occlusion of a
major coronary artery previously affected by
atherosclerosis. This causes a full thickness damage of
heart muscle.

Symptoms of NSTEMI vs STEMI

There is no difference between NSTEMI and

STEMI in clinical presentation. In both cases,

patients usually present with similar type of
symptoms such as chest pain, nausea, vomiting,
sweating, breathing difficulty.

ECG of NSTEMI vs STEMI

The usual ECG findings of NSTEMI are ST-segment

depression or T-wave inversion. NSTEMI does not

show ST segment elevation in ECG (due to partial
thickness injury of heart muscle) and later does not
progress to a Q-wave. For this reason, it is also
called a nonQ-wave myocardial infarction (NQMI).
On the other hand, STEMI shows ST segment
elevation in ECG (due to full thickness injury of heart
muscle) and later progress to a Q-wave. For this
reason, it is also called a Q-wave myocardial
infarction (QWMI). The ultimate ECG findings of
STEMI are ST-segment elevation, pathological Qwave formation and T-wave inversion.

ECG findings of NSTEMI and

STEMI

Cardiac markers of NSTEMI vs STEMI:

Cardiac markers including CK-MB (creatine kinase myocardial
band), troponin I and troponin T, all elevate both in cases. But
the elevation of these markers is often mild in NSTEMI
compared with STEMI.
Diagnosis of NSTEMI vs STEMI:
The diagnosis of a NSTEMI is based on a typical history of
chest pain, no ST segment elevation in ECG plus elevation of
cardiac markers in serum, and the diagnosis of a STEMI is
based on a typical history of chest pain, ST segment elevation
in ECG plus elevation of cardiac markers in serum.
Complications of NSTEMI vs STEMI:
Complications occur both in cases. But some complications like
cardiogenic shock, left ventricular failure, severe mitral
regurgitation due to papillary muscle rupture, cardiac
tamponade due to ventricular wall rupture are more in STEMI
(due to full thickness heart muscle damage) than NSTEMI.

Treatment of NSTEMI vs STEMI

Antiplatelets (Aspirin, Clopidogrel, Ticagrelor), anticoagulants

(Enoxaparin, Dalteparin, Fondaparinux), beta-blockers

(atenolol, metoprolol, bisoprolol), nitrates (isosorbide
dinitrate, glyceryl trinitrate), statins (atorvastatin, rosuvastatin,
simvastatin, pitavastatin), ACE inhibitors (ramipril, enalapril,
captopril, lisinopril) or ARBs (valsartan, candesartan,
losartan, olmesartan) are given both in NSTEMI and STEMI.
In case of reperfusion therapy, primary PCI (percutaneous
coronary intervention) is the treatment of choice for STEMI.
Where primary PCI cannot be achieved within 120 minutes of
diagnosis or PCI is not available, thrombolytic therapy such
as streptokinase, tenecteplase, alteplase or reteplase should
be given.

 Early coronary angiography and revascularization, either

by PCI or by CABG (coronary artery bypass grafting) is

the treatment of choice for medium to high risk patients
with NSTEMI.
Drug treatment is appropriate in low risk patients with
NSTEMI, and coronary angiography and revascularization
reserved for those who fail to settle with drug treatment
Thrombolytic therapy is harmful in NSTEMI. The
aggregate data suggest that patients with NSTEMI may
be put at risk of reinfarction if thrombolytic therapy is
used.

Prognosis of NSTEMI vs STEMI

Short-term (in-hospital or one month) mortality is lower in

NSTEMI (3-5%) compared to STEMI (10-15%). Re-infarction

rate (further heart attack) is higher in NSTEMI (15-25%) after
hospital discharge compared to STEMI (5-8%). Long-term
mortality is similar or higher in NSTEMI compared to STEMI
(two year mortality is approximately 30% in both cases).

http://nstemi.org/nstemi-vs-stemi/

ASUHAN
KEPERAWATAN

Assessment

Primary Assessment for Acute Myocardial Infarction

Airway
Blockage or accumulation of secretions
Wheezing or crackles
Breathing
Shortness of breath with mild activity or rest
Respiration more than 24 x / min, irregular rhythm shallow
Ronchi, crackles
The expansion of the chest is not full
Use of auxiliary respiratory muscles
Circulation
Weak pulse, irregular
Tachycardia
Blood pressure increase / decrease
Edema
Acral cold
Pale skin, cyanosis
Decreased urine output

Secondary Assessment Acute Myocardial Infarction (AMI)

Activities
Symptoms:

Weakness
Fatigue
Can not sleep
Settled lifestyle
No regular exercise schedule

Signs:
Tachycardia
Dyspnea at rest or activity

Circulation
Signs:
Blood pressure: normal / up / down. Postural changes recorded from
the bed to sit or stand
Pulse: normal, full or not strong or weak / strong quality with slow
capillary filling, irregular (dysrhythmias)
Heart sound: an extra heart sound: S3 or S4 may indicate heart failure
or decreased contractility / complaints ventricle
Murmur: If there are shows valve failure or dysfunction of heart
muscle
Friction: suspected pericarditis
Heart rhythm can be regular or irregular
Edema: juguler venous distention, edema dependent, peripheral,
general edema, cracles may exist with heart failure or ventricular
Color: Pale or cyanotic, flat nail, on mucous membranes or lips

DIAGNOSA KEPERAWATAN

Acute Pain
May be related to
Tissue ischemia (coronary artery occlusion)
Possibly evidenced by
Reports of chest pain with/without radiation
Facial grimacing
Restlessness, changes in level of consciousness
Changes in pulse, BP
Desired Outcomes
Verbalize relief/control of chest pain within appropriate time frame for
administered medications.
Display reduced tension, relaxed manner, ease of movement.
Demonstrate use of relaxation techniques.

Nursing Interventions

Rationale
Variation of appearance and behavior of
patients in pain may present a challenge
in assessment. Most patients with an
Monitor/document characteristics of pain, acute MI appear ill, distracted, and
noting verbal reports, nonverbal cues
focused on pain. Verbal history and
(e.g., moaning, crying, restlessness,
deeper investigation of precipitating
diaphoresis, clutching chest , rapid
factors should be postponed until pain is
breathing), and hemodynamic response relieved. Respirations may be increased
(BP/heart rate changes).
as a result of pain and associated
anxiety; release of stress-induced
catecholamines increases heart rate and
BP.
Obtain full description of pain from
patient including location, intensity (0
10), duration, characteristics
(dull/crushing), and radiation. Assist
patient to quantify pain by comparing it
to other experiences.

Pain is a subjective experience and must

be described by patient. Provides
baseline for comparison to aid in
determining effectiveness of therapy,
resolution/progression of problem.

Review history of previous angina,

anginal equivalent, or MI pain. Discuss
family history if pertinent.

Delay in reporting pain hinders pain

relief/may require increased dosage of
medication to achieve relief. In addition,
severe pain may induce shock by
stimulating the sympathetic nervous
system, thereby creating further damage
and interfering with diagnostics and
relief of pain.

Instruct patient to report pain

immediately.Provide quiet environment,
calm activities, and comfort measures

Decreases external stimuli, which may

aggravate anxiety and cardiac strain,
limit coping abilities and adjustment to

Hypotension/respiratory depression can

occur as a result of narcotic
Check vital signs before and after
administration. These problems may
narcotic medication.
increase myocardial damage in presence
of ventricular insufficiency.
Increases amount of oxygen available for
Administer supplemental oxygen by
myocardial uptake and thereby may
means of nasal cannula or face mask, as
relieve discomfort associated with tissue
indicated.
ischemia.
Nitrates are useful for pain control by
coronary vasodilating effects, which
increase coronary blood flow and
myocardial perfusion. Peripheral
vasodilation effects reduce the volume of
blood returning to the heart (preload),
thereby decreasing myocardial workload
and oxygen demand.Important secondline agents for pain control through
effect of blocking sympathetic
Administer medications as
stimulation, thereby reducing heart rate,
indicated:Antianginals, e.g., nitroglycerin
systolic BP, and myocardial oxygen
(Nitro-Bid, Nitrostat, Nitro-Dur),
demand.May be given alone or with
isosorbide denitrate (Isordil),
nitrates.Note:beta-blockers may be
mononitrate (Imdur)Beta-blockers, e.g.,
contraindicated if myocardial
atenolol (Tenormin), pindolol(Visken),
contractility is severely impaired,
propranolol (Inderal), nadolol (Corgard),
because negative inotropic properties
metoprolol (Lopressor)
can further reduce contractility.

Although intravenous (IV) morphine is

Analgesics, e.g., morphine, meperidine
the usual drug of choice, other injectable
(Demerol)
narcotics may be used in acute-

Activity Intolerance
May be related to
Imbalance between myocardial oxygen supply and demand
Presence of ischemia/necrotic myocardial tissues
Cardiac depressant effects of certain drugs (beta-blockers, antidysrhythmics)
Possibly evidenced by
Alterations in heart rate and BP with activity
Development of dysrhythmias
Changes in skin color/moisture
Exertional angina
Generalized weakness
Desired Outcomes
Demonstrate measurable/progressive increase in tolerance for activity with heart
rate/rhythm and BP within patients normal limits and skin warm, pink, dry.
Report absence of angina with activity.

Nursing Interventions
Record/document heart rate and
rhythm and BP changes before,
during, and after activity, as
indicated. Correlate with reports of
chest pain/shortness of breath.

Rationale
Trends determine patients response
to activity and may indicate
myocardial oxygen deprivation that
may require decrease in activity
level/return to bedrest, changes in
medication regimen, or use of
supplemental oxygen.

Encourage rest (bed/chair) initially.

Thereafter, limit activity on basis of
pain/ adverse cardiac response.
Provide nonstress diversional
activities.

Reduces myocardial workload/oxygen

consumption, reducing risk of
complications (e.g., extension of MI).

Instruct patient to avoid increasing

abdominal pressure, e.g., straining
during defecation.

Activities that require holding the

breath and bearing down (Valsalva
maneuver) can result in bradycardia
(temporarily reduced cardiac output)
and rebound tachycardia with
elevated BP.

Explain pattern of graded increase of

activity level, e.g., getting up to
commode or sitting in chair,
progressive ambulation, and resting
after meals.

Progressive activity provides a

controlled demand on the heart,
increasing strength and preventing
overexertion.

Review signs/symptoms reflecting

intolerance of present activity level

Palpitations, pulse irregularities,

development of chest pain, or
dyspnea may indicate need for

Tujuan dan kriteria hasil

1. Menunjukan penghematan energi dengan indikator :
Aktivitas dan istirahat seimbang
Mengenali keterbatasan energi
Menggunakan teknik konservasi energi
Nutrisi adekuat
Mempertahankan level yang adekuat untuk aktivitas
2. Toleransi aktivitas
Kriteria :
SaO2 sebagai respon terhadap aktivitas dbn
HR sebagai respon terhadap aktivitas dbn
RR sebagai respon terhadap aktivitas dbn
TD sistolik sebagai respon terhadap aktivitas dbn
TD diastolik sebagai respon terhadap aktivitas dbn
Warna kulit normal
Menunjukan kemampuan dalam melakukan ADLs

a. Terapi aktivitas
Kaji kemampuan pasien melakukan aktivitas
Evaluasi motivasi dan keinginan pasien u/ meningkatkan aktivitas
Jelaskan pada pasien manfaat beraktivitas secara bertahap
Bantu dalam pemenuhan aktivitas perawatan diri jika pasien belum
dapat mentoleransi aktivitas tsb.
Orientasikan pasien beraktivitas secara bertahap sesuai toleransi
Tetap sertakan O2 selama beraktivitas
Bantu pasien mengidentifikasi pilihan aktivitas
Berikan reinforcement u/ peningkatan aktivitas

Manajemen energi
Tentukan penyebab keletihan
Rencanakan aktivitas pada saat ps mempunyai energi yg cukup
Berikan periode istirahat selama beraktivitas
Monitor TV sebelum, selama dan sesudah beraktivitas
Catat respon kardiorespirasi setelah melakukan aktivitas.
Monitor pola tidur pasien
Rencanakan periode istirahat adekuat sesuai jadwal harian pasien
Lakukan langkah-langkah untuk meningkatkan kualitas dan kuantitas
periode tidur dan istirahat pasien.
Bantu klien dengan tindakan untuk menyimpan kekuatan, seperti
istirahat sebelum dan sesudah aktifitas, misalnya makan
Pantau asupan nutrisi untuk memastikan keadekuatan sumber energi
Ajarkan tentang pengaturan aktivitas dan teknis manajemen waktu
untuk mencegah kelelahan
Rujuk ke ahli gizi untuk merencanakan makanan untuk meningkatkan
asupan energi

Fear/Anxiety

May be related to
Threat to or change in health and socioeconomic status
Threat of loss/death
Unconscious conflict about essential values, beliefs, and goals of life
Possibly evidenced by
Fearful attitude
Apprehension, increased tension, restlessness, facial tension
Uncertainty, feelings of inadequacy
Somatic complaints/sympathetic stimulation
Focus on self, expressions of concern about current and future events
Fight (e.g., belligerent attitude) or flight behavior
Desired Outcomes
Recognize feelings.
Identify causes, contributing factors.
Verbalize reduction of anxiety/fear.
Demonstrate positive problem-solving skills.
Identify/use resources appropriately.

Nursing Interventions

Rationale
Coping with the pain and emotional
trauma of an MI is difficult. Patient may
fear death and/or be anxious about
immediate environment. Ongoing anxiety
Identify and acknowledge patients
(related to concerns about impact of heart
perception of threat/situation. Encourage
attack on future lifestyle, matters left
expressions of, and do not deny feelings
unattended/unresolved, and effects of
of, anger, grief, sadness, fear.
illness on family) may be present in
varying degrees for some time and may
be manifested by symptoms of
depression.
Research into survival rates between type
A and type B individuals and the impact of
Note presence of hostility, withdrawal,
denial has been ambiguous; however,
and/or denial (inappropriate affect or
studies show some correlation between
refusal to comply with medical regimen). degree/
expression of anger or hostility and an
increased risk for MI.
Patient and SO can be affected by the
Maintain confident manner (without false anxiety/uneasiness displayed by health
reassurance).
team members. Honest explanations can
alleviate anxiety.
Patient may not express concern directly,
Observe for verbal/nonverbal signs of
but words/actions may convey sense of
anxiety, and stay with patient. Intervene if agitation, aggression, and hostility.
patient displays destructive behavior.
Intervention can help patient regain
control of own behavior.
Denial can be beneficial in decreasing
anxiety but can postpone dealing with the

Answer all questions factually.

Provide consistent information;
repeat as indicated.

Encourage patient/SO to
communicate with one another,
sharing questions and concerns.
Provide privacy for patient and SO.
Provide rest periods/uninterrupted
sleep time, quiet surroundings, with
patient controlling type, amount of
external stimuli.
Support normality of grieving
process, including time necessary for
resolution.

Accurate information about the

situation reduces fear, strengthens
nurse-patient relationship, and
assists patient/SO to deal realistically
with situation. Attention span may be
short, and repetition of information
helps with retention.
Sharing information elicits
support/comfort and can relieve
tension of unexpressed worries.
Allows needed time for personal
expression of feelings; may enhance
mutual support and promote more
adaptive behaviors.
Conserves energy and enhances
coping abilities.

Can provide reassurance that

feelings are normal response to
situation/perceived changes.
Increased independence from staff
promotes self-confidence and
Encourage independence, self-care,
reduces feelings of abandonment
and decision making within accepted
that can accompany transfer from
treatment plan.
coronary unit/discharge from
hospital.

Risk for Decreased Cardiac

Risk factors may include
Output

Changes in rate, rhythm, electrical conduction

Reduced preload/increased SVR (Systemic Vascular
Resistance)
Infarcted/dyskinetic muscle, structural defects, e.g., ventricular
aneurysm, septal defects
Possibly evidenced by
[Presence of signs and symptoms is needed to establish and actual
diagnosis.]
Desired Outcomes
Maintain hemodynamic stability, e.g., BP, cardiac output within normal
range, adequate urinary output, decreased frequency/absence of
dysrhythmias.
Report decreased episodes of dyspnea, angina.
Demonstrate an increase in activity tolerance.

Nursing Interventions

Rationale
Hypotension may occur related to
ventricular dysfunction, hypoperfusion of
the myocardium, and vagal stimulation.
Auscultate BP. Compare both arms and
However, hypertension is also a common
obtain lying, sitting, and standing
phenomenon, possibly related to pain,
pressures when able.
anxiety, catecholamine release, and/or
preexisting vascular problems. Orthostatic
(postural) hypotension may be associated
with complications of infarct, e.g., HF.
Decreased cardiac output results in
Evaluate quality and equality of pulses, as diminished weak/thready pulses.
indicated.
Irregularities suggest dysrhythmias, which
may require further evaluation/monitoring.

Auscultate heart sounds:Note

development of S3, S4;Presence of
murmurs/rubs. Auscultate breath sounds.

S3is usually associated with HF, but it may

also be noted with the mitral insufficiency
(regurgitation) and left ventricular
overload that can accompany severe
infarction. S4may be associated with
myocardial ischemia, ventricular
stiffening, and pulmonary or systemic
hypertension.Indicates disturbances of
normal blood flow within the heart, e.g.,
incompetent valve, septal defect, or
vibration of papillary muscle/chordae
tendineae (complication of MI). Presence
of rub with an infarction is also associated
with inflammation, e.g., pericardial
effusion and pericarditis.Crackles
reflecting pulmonary congestion may
develop because of depressed myocardial

Overexertion increases oxygen

consumption/demand and can
compromise myocardial function.
Large meals may increase myocardial
workload and cause vagal
stimulation, resulting in
Provide small/easily digested meals. bradycardia/ectopic beats. Caffeine
Limit caffeine intake, e.g., coffee,
is a direct cardiac stimulant that can
chocolate, cola.
increase heart rate.Note:New
guidelines suggest no need to
restrict caffeine in regular coffee
drinkers.
Note response to activity and
promote rest appropriately.

Sudden coronary occlusion, lethal

dysrhythmias, extension of infarct,
Have emergency equipment/
and unrelenting pain are situations
medications available.
that may precipitate cardiac arrest,
requiring immediate life-saving
therapies/transfer to CCU.
Increases amount of oxygen
Administer supplemental oxygen, as available for myocardial uptake,
indicated.
reducing ischemia and resultant
cellular irritation/dysrhythmias.
Cardiac index, preload/afterload,
contractility, and cardiac work can be
measured noninvasively with
Measure cardiac output and other
thoracic electrical bioimpedance
functional parameters as
(TEB) technique. Useful in evaluating

Provides information regarding

progression/resolution of infarction,
Review serial ECGs.
status of ventricular function,
electrolyte balance, and effects of
drug therapies.
May reflect pulmonary edema
Review chest x-ray.
related to ventricular dysfunction.
Enzymes monitor
resolution/extension of infarction.
Presence of hypoxia indicates need
Monitor laboratory data, e.g.,
for supplemental oxygen. Electrolyte
cardiac enzymes, ABGs, electrolytes. imbalance, e.g.,
hypokalemia/hyperkalemia,
adversely affects cardiac
rhythm/contractility.
Dysrhythmias are usually treated
symptomatically, except for PVCs,
which are often treated
prophylactically. Early inclusion of
ACE inhibitor therapy (especially in
Administer antidysrhythmic drugs as presence of large anterior MI,
indicated.
ventricular aneurysm, or HF)
enhances ventricular output,
increases survival, and may slow
progression of HF.Note:Use of
routine lidocaine is no longer

Penurunan curah jantung b/d

Iskemia ventrikuler
DS:
-Nyeri dada
-Dispneu
-Kelelahan
-Nafas pendek
-Kelemahan
DO:
-Enzim jantung tidak normal
-Perubahan status mental
-Aritmia
-Penurunan nadi perifer
-Perubahan EKG
-Nafas pendek/ sesak nafas
-Bunyi jantung S3 atau S4

NOC
Cardiac Pump effectiveness
Circulation Status
Vital Sign Status
Tissue perfusion: perifer

Menunjukan keefektifan curah jantung, indikator:

Tanda Vital dalam rentang normal (Tekanan darah, Nadi, respirasi)
Dapat mentoleransi aktivitas
tidak ada kelelahan
Tidak ada penurunan kesadaran
AGD dalam batas normal
Status sirkulasi adekuat, indikator :
TD sistolik dan diastolik dbn
Denyut jantung dbn
Hipotensi ortostatik tidak ada
Gas darah dbn
Status kognitif dbn

NIC : Cardiac care : akut

monitor irama dan denyut jantung, auskultasi bunyi crakles

pada paru-paru, atau suara-suara lainnya yang ditemukan
monitor intake dan output, jika pasien dalam penyakit akut,
ukur haluaran urin /jam catat adanya penurunan jumlah urin.
Ajarkan untuk melaporkan dan menggambarkan awitan
palpitasi, nyeri
berikan makanan dengan pembatasan sodium, dan rendah
kolesterol. Berikan kopi dalam jumlah yang sedikit jika tidak
terdapat disritmia
berikan lingkungan yang tenang dengan minimalkan stressor
dan gangguan yang tidak perlu
kaji BB pasien setiap hari
monitor fungsi BAB. Berikan pelunak feses. Beri peringatan
kepada pasien supaya jangan mengejan saat BAB
Kolaborasi pemberian obat aritmia, inotropik dan vasodilator

Risk for Ineffective Tissue

Perfusion
Risk factors may include
Reduction/interruption of blood flow, e.g., vasoconstriction,
hypovolemia/shunting, and thromboembolic formation
Possibly evidenced by
[Not applicable; presence of signs and symptoms establishes
an actual diagnosis.]
Desired Outcomes
Demonstrate adequate perfusion as individually appropriate, e.g., skin
warm and dry, peripheral pulses present/strong, vital signs within
patients normal range, patient alert/oriented, balanced I&O, absence of
edema, free of pain/discomfort.

Nursing Interventions
Investigate sudden changes or continued
alterations in mentation, e.g., anxiety,
confusion, lethargy, stupor.
Inspect for pallor, cyanosis, mottling,
cool/clammy skin. Note strength of
peripheral pulse.

Monitor respirations, note work of

breathing.

Monitor intake, note changes in urine

output. Record urine specific gravity as
indicated.

Assess GI function, noting anorexia,

decreased/absent bowel sounds,
nausea/vomiting, abdominal distension,
constipation.

Encourage active/passive leg exercises,

avoidance of isometric exercises.

Rationale
Cerebral perfusion is directly related to
cardiac output and is also influenced by
electrolyte/acid-base variations, hypoxia,
and systemic emboli.
Systemic vasoconstriction resulting from
diminished cardiac output may be
evidenced by decreased skin perfusion
and diminished pulses.
Cardiac pump failure and/or ischemic pain
may precipitate respiratory distress;
however, sudden/continued dyspnea may
indicate thromboembolic pulmonary
complications.
Decreased intake/persistent nausea may
result in reduced circulating volume,
which negatively affects perfusion and
organ function. Specific gravity
measurements reflect hydration status
and renal function.
Reduced blood flow to mesentery can
produce GI dysfunction, e.g., loss of
peristalsis. Problems may be
potentiated/aggravated by use of
analgesics, decreased activity, and dietary
changes.
Enhances venous return, reduces venous
stasis, and decreases risk of
thrombophlebitis; however, isometric
exercises can adversely affect cardiac

Indicators of organ perfusion/function.

Monitor laboratory data, e.g., ABGs, BUN, Abnormalities in coagulation may occur
creatinine, electrolytes, coagulation
as a result of therapeutic measures (e.g.,
studies (PT, aPTT, clotting times).
heparin/Coumadin use and some cardiac
drugs).
Reduces mortality in MI patients, and is
taken daily. Aspirin also reduces coronary
reocclusion after percutaneous
transluminal coronary angioplasty
Administer medications as indicated:
(PTCA). ReoPro is an IV drug used as an
Antiplatelet agents, e.g., aspirin,
adjunct to PTCA for prevention of acute
abciximab (ReoPro), clopidogrel (Plavix); ischemic complications.Low-dose heparin

is given during PTCA and may be given

Anticoagulants, e.g., heparin/enoxaparin prophylactically in high-risk patients
(Lovenox);
(e.g., atrial fibrillation, obesity,

ventricular aneurysm, or history of

Oral anticoagulants, e.g., anisindione
thrombophlebitis) to reduce risk of
(Miradon), warfarin (Coumadin);
thrombophlebitis or mural thrombus
Cimetidine (Tagamet), ranitidine
formation.Used for prophylaxis and
(Zantac), antacids;
treatment of thromboembolic

complications associated with MI.Reduces

or neutralizes gastric acid, preventing
discomfort and gastric irritation,
especially in presence of reduced
mucosal circulation.
Thrombolytic therapy is the treatment of
choice (when initiated within 6 hr) to
dissolve the clot (if that is the cause of
Assist with reperfusion
the MI) and restore perfusion of the
therapy:Administer thrombolytic agents, myocardium.This procedure is used to

Deficient Knowledge
May be related to
Lack of information/misunderstanding of medical condition/therapy needs
Unfamiliarity with information resources
Lack of recall
Possibly evidenced by
Questions; statement of misconception
Failure to improve on previous regimen
Development of preventable complications
Desired Outcomes
Verbalize understanding of condition, potential complications, individual risk factors,
and function of pacemaker (if used).
Verbalize understanding of therapeutic regimen.
List desired action and possible adverse side effects of medications.
Correctly perform necessary procedures and explain reasons for actions.

Nursing Interventions
Rationale
Assess patient/SO level of knowledge Necessary for creation of individual
and ability/desire to learn.
instruction plan.
Be alert to signs of avoidance, e.g., Reinforces expectation that this will
changing subject away from
be a learning experience.
information being presented or
Verbalization identifies
extremes of behavior (withdrawal/
misunderstandings and allows for
euphoria).
clarification.

Present information in varied

learning formats, e.g., programmed
books, audiovisual tapes, questionand-answer sessions, group
activities.

Reinforce explanations of risk

factors, dietary/activity restrictions,
medications, and symptoms
requiring immediate medical
attention.
Encourage identification/ reduction
of individual risk factors, e.g.,
smoking/alcohol consumption,
obesity.

Natural defense mechanisms, such

as anger or denial of significance of
situation, can block learning,
affecting patients response and
ability to assimilate information.
Changing to a less formal/structured
style may be more effective until
patient/SO is ready to accept/deal
with current situation.
Using multiple learning methods
enhances retention of material.
Provides opportunity for patient to
retain information and to assume
control/participate in rehabilitation
program.

Review programmed increases in

levels of activity. Educate patient
regarding gradual resumption of
activities, e.g., walking, work,
recreational and sexual activity.
Provide guidelines for gradually
increasing activity and instruction
regarding target heart rate and pulse
taking, as appropriate.

These activities greatly increase

cardiac workload and myocardial
oxygen consumption and may
adversely affect myocardial
contractility/output.

Gradual increase in activity increases

strength and prevents overexertion,
may enhance collateral circulation,
Identify alternative activities for
and allows return to normal
bad weather days, such as
lifestyle.Note:Sexual activity can be
measured walking in house or
safely resumed once patient can
shopping mall.
accomplish activity equivalent to
climbing two flights of stairs without
adverse cardiac effects.
Pulse elevations beyond established
Review signs/ symptoms requiring
limits, development of chest pain, or
reduction in activity and notification
dyspnea may require changes in
of healthcare provider.
exercise and medication regimen.
Differentiate between increased
heart rate that normally occurs
during various activities and
Pulse elevations beyond established
worsening signs of cardiac stress

Stress importance of follow-up

care, and identify community
resources/support groups, e.g.,
cardiac rehabilitation programs,
coronary clubs, smoking
cessation clinics.

Emphasize importance of
contacting physician if chest pain,
change in anginal pattern, or
other symptoms recur.
Stress importance of reporting
development of fever in
association with diffuse/atypical
chest pain (pleural, pericardial)
and joint pain.

Reinforces that this is an

ongoing/continuing health
problem for which
support/assistance is available
after discharge.Note:After
discharge, patients encounter
limitations in physical functioning
and often incur difficulty with
emotional, social, and role
functioning requiring ongoing
support.
Timely evaluation/ intervention
may prevent complications.

Post-MI complication of
pericardial inflammation
(Dresslers syndrome) requires
further medical
evaluation/intervention.
Depressed patients have a
greater risk of dying 618 mo
Encourage patient/SO to share
following a heart attack. Timely
concerns/ feelings. Discuss signs intervention may be
of pathological depression versus beneficial.Note:Selective
transient feelings frequently
serotonin reuptake inhibitors